Financial/nonfi nancial disclosures: The authors have reported to CHEST the following confl icts of interest: Dr Somers has served as a consultant for ResMed, Respironics, Medtronic, GlaxoSmith-Kline, Sepracor, Boston Scientifi c, and Cardiac Concepts. He has received research grants from the ResMed Foundation, the Respironics Sleep and Breathing Foundation, ELA Medical, and Select Research, Inc. Dr Ishida and Dr Kato have reported no confl icts of interest that exist with any companies/organizations whose products or services may be discussed in this article.

To the Editor:

We appreciate some of the comments in the letter by Ryan and McNicholas, but we are surprised and disappointed by misrepresentations of our work, as noted in the latter paragraphs of our response below. They suggest that we understate the controversy regarding the relationship between obstructive sleep apnea (OSA) and C-reactive protein (CRP). We agree that we could have addressed further the question of whether OSA raises CRP. However, the focus of our study1 was the effect of continuous positive airway pressure (CPAP) on CRP. We specify clearly that “the available data are controversial,” and we refer to “the inconsistency found in prior studies.” Indeed, it is this very lack of consensus that strengthens the justification for our study. Our manuscript was not intended, nor should it be misinterpreted, as any kind of comprehensive review.

We did not cite the Ryan and colleagues review,2 nor the randomized study by Kohler et al,3 as both were published after acceptance of our manuscript. Regarding whether OSA causes an increase in CRP, Ryan and McNicholas fail to clarify that only 111 subjects in the Sleep Cohort Study4 had an apnea-hypopnea index > 15, with far fewer having an apnea-hypopnea index approaching 46, the approximate mean in our 55 subjects. Furthermore, they ignore several other relevant studies cited in Table 1.5-7 We agree that whether it is obesity or OSA, or an interaction between the two, that contributes to the elevated CRP awaits a definitive answer. Nevertheless, the issue may be of considerably less relevance, given recent data arguing against a causal role of CRP in coronary artery disease.8

Their criticism of the “small patient numbers (n = 15) in the poor compliance group” is somewhat justified. However, publishing data from small sample sizes is not outside the norm, as exemplified in many studies by Ryan et al,9-13 which report data from as few as eight to 10 subjects.11,12 Indeed, our study had a larger overall sample size than their similar but much shorter (6 weeks) study of CPAP effects on CRP,10 which is not cited in their letter. On the other hand, the question of outliers is very reasonable. Even after excluding these three subjects, CRP was reduced (P = .0123).

In comparing our data with the excellent study by Kohler et al,3 Ryan and McNicholas overlook several important and fundamental differences between our studies, as outlined in Table 2. The “great interest” with which they read our work is hard to reconcile with their assertion that we “do not provide important baseline and follow-up information on potential confounding variables that may have influenced CRP levels such as medications and changes in lipid and glucose profiles at follow-up.” Lipid and glucose data were in fact presented in Table 1 (baseline data) and Table 2 (changes after therapy).1 Furthermore, we state explicitly that patients using statins were excluded and that “we did not add or change any medications” during the study.

It was in the high CRP group in whom Ishida et al noted the clearest change.

Studied effects of 1 mo of CPAP

Studied effects of 6 mo of CPAP

The longer follow-up may have enabled us to show differences consistent with Steiropoulos et al,14 who also found a decrease in CRP after 6 mo of CPAP; regarding randomized studies, Drager et al15 also found a significant decrease in CRP, but again after 4 mo of CPAP therapy.

Medication-related issues not directly addressed

Patients on statins excluded; no medications added or changed during study

…

CPAP = continuous positive airway pressure. See Table 1 for expansion of the other abbreviation.

Ryan and McNicholas seem unconcerned that neither lipids nor glucose nor changes in statins/medications are described in the Kohler et al manuscript, but inappropriately chastise us for this. More remarkable is that they make no mention of either statins or changes in lipids and glucose in their own study of CRP before and after CPAP.10 Criticism that is thoughtful, fair, and well-informed is always welcome. Otherwise it is simply tedious in the reading, time consuming in the rebuttal, and adds little that is constructive to the literature.

It was in the high CRP group in whom Ishida et al noted the clearest change.

Studied effects of 1 mo of CPAP

Studied effects of 6 mo of CPAP

The longer follow-up may have enabled us to show differences consistent with Steiropoulos et al,14 who also found a decrease in CRP after 6 mo of CPAP; regarding randomized studies, Drager et al15 also found a significant decrease in CRP, but again after 4 mo of CPAP therapy.

Medication-related issues not directly addressed

Patients on statins excluded; no medications added or changed during study

…

CPAP = continuous positive airway pressure. See Table 1 for expansion of the other abbreviation.

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